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      • KCI등재

        사암침법(舍巖鍼法)의 보사수기법(補瀉手技法)에 관한 연구(硏究)

        안정란 ( Jeong Ran Ahn ),이인선 ( In Seon Lee ) 한방재활의학과학회 2009 한방재활의학과학회지 Vol.19 No.2

        Objectives: The purpose of this study is what Saamchimbeop`s method of reinforcement and reduction. Methods: 1. We reffered to the Bo-Sa method of DongeuiBo-gam(東醫寶鑑), Uihakim-mun(醫學入門), Uihakjeong-jeon(醫學正傳), Chimgugyeongheom-bang(鍼灸經驗方), Biaoyou-fu(標幽賦) in Cimgudaeseong(鍼灸大成), Nei-Jing(內經). 2. We make a conjecture that Zheng(正), Ying(迎), Sui(隨), Xie(斜) Yingzheng(迎正), Duo(奪), Zhenghuoxie(正或斜), Wen(溫), Liang(凉), JongYang-Inyin (從陽引陰) in Saamchimbeop are another expression of method of reinforcement and reduction and compared with the method of reinforcement and reduction of DongeuiBo-gam(東醫寶鑑), Uihakim-mun(醫學入門), Uihakjeong-jeon(醫學正傳), Chimgugyeongheom-bang(鍼灸經驗方), Biaoyou-fu(標幽賦) in Cimgudaeseong(鍼灸大成), Nei-Jing(內經). Results: 1. Zheng(正) and Xie(斜) are angle of acupuncture manipulation. The descending inserting of Yang-meridian is acupuncture manipulation for the Tonifying effect(補法) and the direct inserting of Yin-meridian is the Dispersing effect(瀉法). 2. JongYang-Inyin(從陽引陰) is the contralateral acupuncture. 3. Ying(迎) and Sui(隨) in the Saamchimbeop are same meaning the method of reinforcement and reduction(補瀉手技法). 4. Saamchimbeop`s the final aim is the Wen-Liang(溫凉) according to the disease strong and weak in the Ohaeng-seo of Saam-acupuncture. Conclusions: Saamchimbeop`s method of reinforcement and reduction is reinforcement-reduction by lifting and thrusting the needle, breathing reinforcement-reduction method, reinforcing and reducing achieved by rapid and slow insertion and withdrawing of the needles, reinforcement and reduction by opening and closing of needles with contralateral acupuncture by Yin-meridian or Yang-meridian. Saamchimbeop`s the final aim is the Wen-Liang(溫凉) according to the disease strong and weak.

      • KCI등재

        고지방식이 비만마우스에서 월비가출탕(越婢加朮湯)이 식이효율과 내장지방에 미치는 영향

        안정란 ( Jeong Ran An ),강연경 ( Yeon Kyeong Kang ),장동호 ( Dong Ho Chang ),이인선 ( In Seon Lee ),신순식 ( Soon Shik Shin ),정해경 ( Hae Gyeong Jeong ),이희영 ( Hee Young Lee ),이혜림 ( Hye Rim Lee ) 한방재활의학과학회 2011 한방재활의학과학회지 Vol.21 No.1

        Objectives: This study was undertaken to verify the effects of Wolbigachul-tang 1(WBCEx1) on obesity using high fat diet-induced male mice and to investigate the molecular mechanisms involved. Methods: 8-week old C57BL/6 mice were divided into 5 groups; lean control, obese control, WBCEx1, 2, 3. After mice were treated with WBCE x1(water extract), 2(30% ethanol extract), 3(water extract; Ephedra sinica Stapf., Gypsum fibrosum) for 12 weeks, body weight gain, feeding efficiency ratio, plasma lipid and glucose metabolism, the messenger RNA(mRNA) expression of peroxisome proliferator activated receptor(PPAR)α target genes were measured. In addition, PPARα target gene expression was examined in liver, white adipose tissue and skeletal muscle. Results :1. WBCEx1-treated mice had significantly lower body weight gain and feeding efficiency ratio. 2. Consistent with the effects on body weight gain, WBCEx1 decreased the weights of epididymal and retroperitoneal white adipose tissue, inguinal subcutaneous adipose tissue, and brown adipose tissue. 3. WBCEx1 significantly decreased plasma triglyceride and total cholesterol levels. 4. The size of adipocytes were significantly decreased by WBCEx1, whereas the adipocyte number per unit area was increased. Hepatic lipid accumulation was decreased by WBCEx1. 5. WBCEx1 did not affect the mRNA expression of PPARα target genes in liver, adipose tissue, and skeletal muscle. 6. Plasma asparate aminotransferase(AST), alanine aminotransferase(ALT), blood urea nitrogen(BUN) and creatine concentrations were in the physiological range. Liver and kidney weights were significantly lower following WBCEx treatment compared with obese controls, indicating that WBCEx does not show any toxic effects on liver and kidney. Conclusions: These results suggest that WBCEx1-induced body weight reduction is associated with appetite control and mediated by a mechanism other than the activation of PPARα.

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